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PO-59 - Hemorheologic disturbances as thrombosis risk factor in patients with some myeloproliferative neoplasms.

INTRODUCTION: In today's antithrombotic prevention we forget that hemorheologic abnormalities are part of Virchow's triad. Isn't this one of reasons that venous thromboembolism (VTE) including catheter-related thrombosis (CRT) retain high frequency despite of modern antithrombotic therapy?

AIM: The aim was to investigate rheological behavior of blood in patients with some myeloproliferative neoplasms.

MATERIALS AND METHODS: The study included 16 adults with Polycythemia Vera (PV), 42 young with acute lymphoblastic leukemia (ALL), and 67 healthy donors as control group. Of patients 38% had thrombosis. We measured plasma viscosity, and whole blood viscosity (WBV) by shear rate from 300 to 5 s-1. Then indices were calculated for erythrocyte aggregation, and deformability, and non-Newtonian behavior of blood. Hematocrit, erythrocytes count, erythrocyte indices, leukocyte count, fibrinogen and B-type natriuretic peptide (BNP) were analyzed simultaneously.

RESULTS: Increased WBV revealed totally in PV-patients but not by all shear rates in ALL-patients. Unlike donor, in patients WBV values had no equivalence under sequential one sample measurements with a decrease and then an increase of shear rates. We speculated this difference becomes diagnostic meaning like one and by its size. WBV dependent on leukocytes count, on MCH and mainly on MCV. Forty percent of patients had elevated BNP assuming subclinical cardiac dysfunction. The latter explains discoordinated changes in shear stress values required for fully reversible erythrocyte aggregation. As a result, residual units like "erythrocyte-erythrocyte" and/or "erythrocyte-leukocyte" interferes blood stream and violates mechanically blood flow in small vessels. Moreover in PV-patients but not in ALL-patients we found loss of non-Newtonian behavior of blood later than in control group. Both myeloproliferative neoplasms lead to increased erythrocyte aggregation but not impair deformability of red blood cells. In total these facts explains chronic hypoxia in these patients.

CONCLUSIONS: Patients with some myeloproliferative neoplasms has abnormal blood flow properties. Revealed hemorheologic disturbances could be as a trigger to start of VTE or to growth of blood clot in the area of permanent venous catheter. These non-hemocoagulation conditions leaded for thrombus formation makes hemorheologic therapy looking attractive for antithrombotic management. The choice of targeted methods requires to continue this study.

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